rojak Flashcards
type 2 pneumocytes produce?
surfactant ___long ass word___ c______
surfactant dipalmitoylphosphatidyl choline
cause of plasma exudation???
when airway mucosa provoked. airway epithelial cells and endothelial cells exposed to inflammatory mediators (e.g. PAF & histamines), increases permeability, allow for fluid extravasation, macromolecules and cells to escape from blood vessels and into airway walls, interstitial spaces and airway lumen.
cilia description
attachments: apical hools which engage w mucous cytoskeleton: 9 doublets + 2 central microtubules (axoneme) nexin links and dynein arms
which part of inspiration and expiration is effort dependent
the ENTIRE inspiration dumbass and early expiration
late expiration is effort INdependent like a strong women. amt of air breathed out is the same regardless of effort. depends on compliance and elasticity of lungs and chest wall.
fixed obstruction affect what (flow volume loop)
BOTH loops of inspiration and expiration. check notes
variable obstruction got 2 types
- intrathoracic
- extrathoracic
each affect what and how (flow volume loop)
intrathoracic affect expiratory loop (IE)
- most severe in expiration, relieved by inspiration
- due to e.g. excess mucus
extrathoracic affect inspiratory loop (EI)
- severe in inspiratory, relieved by expiration
- due to things e.g. tumour
what is dynamic compression, when does it occur
forced expiration. intrapleural pressure more positive -> intrapleural pressure > airway (alveolar)
pressure
hence, favour airway compression
to what system/part of brain
voluntary -> ?
reflex->?
emotional->?
voluntary -> motor cortex
reflex-> brain stem
emotional -> limbic system
note: locked in syndrome
hemoptysis means what
cough blood
HAPE = high altitude pulmonary edema
use what drug
nifedipine
which fyi, is also a CCB (calcium channel blocker), which should NOT be used with b-blockers
at which rib does the parietal pleura cross the
- midclavicular line
- midaxillary line
- scapular line
*repeat for lung
parietal pleura
- 8th rib
- 10th rib
- 12th rib
lung
- 6th rib
- 8th rib
- 10th rib
isometric contraction vs isotonic contraction
match the feature!
- isovolumetric ventricular contraction/ventricular ejection
- no shortening of muscle fibers/shortening of muscle fibers
- pressure increase, valve close/ enough pressure, valve open
- associated with preload/afterload (graph)
isometric contraction
- isovolumetric ventricular contraction with NO shortening of muscle fibers. pressure keeps increasing due to exertion by surrounding muscles on chamber with valve close.
- length tension graph. more preload more force (Frank Starling relationship)
isotonic contraction
- ventricular ejection, shortening of muscle fibers. once sufficient pressure -> valve open (aortic and pulmonary).
- graph of muscle shortening against amt of AFTERload experienced. more afterload, less muscle shortening
afterload how to measure
use diastolic arterial BP
preload how to measure
end diastolic volume + pressure
OR right atrial pressure
calcium bind what in myofilament for contraction
troponin c
What pulmonary cell type is primarily involved in connective tissue synthesis?
type 2 pneumocytes/epithelial cells
myalgia means what
muscle pain
adenocarcinoma. 特点是什么
papillary tumour. 特点是什么
adeno -> GLANDULAR structure
papillary -> FINGER-LIKE projections
squamous cell carcinoma 特点是什么
highly associated with what
keratinization or intercellular bridges
mutation in tp53 and CDKN2A
Epithelioid histiocytes is what
MACROPHAGES
main cellular components of Granulomatous inflammation
Epithelioid histiocytes and lymphocytes
note: granulomatous inflammation is the macrophage make a shield around TB
KREBS CYCLE
your almost worst nightmare
citrate to isocitrate what enzyme
aconitase dumbass.
kreb cycle
ENZYMESSSSSSSS
oxaloacetate -> citrate -> isocitrate -> a-ketoglutarate -> succincyl coa -> succinate-> fumarate -> malate -> oxaloacetate
- acetyl coa
- aconitase
- isocitrate dhg
- a-ketoglutarate dhg
- succinyl coa synthase
- succinate dgh
- fumarase
- malate dgh
alternaria is what and cause what
plant pathogen. cause allergic rhinitis
which pathway of the 3 allergic thing is just built different
- allergic rhinitis
- asthma
- allergic alveolitis
allergic alveolitis is non IgE mediated while the rest are IgE mediated
allergic alveolitis is IgG mediated
C3a and C5a do what
CHEMOKINES so they CHEMOTAXIS. they activated by proteases then increase inflammation by yelling at the cells that the bacteria is here. aka the modern billboards
classical pathway of complement system is how
1 4 2 3b 5b 6 7 8 9
5b 6 7 8 9 break off form MAC
3b used for opsonisation, bind to macrophage through C3b receptor
C5a C6 C7 C8 C9 make what for what
MAC = membrane attack complex
they attack the bacteria membrane and make a hole so the enzyme and shits can enter the bacteria. so the bacteria die bad bad
alternative pathway how
C3b directly bind, then the rest same same as classical pathway
lectin pathway (complement system) is what
C4 bind to mamose. then just continue from there.
c4 c2 c3b 5b 6 7 8 9
then same same
pyrexia means what
fever
Where is the breast located?
- what region?
- where does it extend from?
situated in superficial fascia of the pectoral region.
extend vertically from the 2nd to the 6th rib in the midclavicular line.
extends horizontally from lateral border of the sternum to the midaxillary line at the level of 4th costal cartilage
retromammary space is what
space that separates the breast from the pectoral fascia (and muscles)
retromammary space got what, for what
loose areolar tissue, allow for free movement of the breast on these muscles
areolar tissue got what, for what
loose connective tissue composed of collagen, elastic fibres and reticular fibres
for: bind skin to muscles beneath, provide support, strength and elasticity to the tissues
mammary gland got what
mammary gland tissue, fibrofatty tissue, connective tissue, blood vessels and lymphatics
lactiferous duct do what
drain each lobule, opens independently into top of nipple
breast blood drains into? (3 veins)
internal thoracic vein, axillary vein (mainly) and intercostal veins, along intercostal neurovascular bundle
suspensory ligaments? (breast)
connective tissue between gland lobules. extend from skin to pectoral fascia.
4 quadrants of the breast?
A. upper outer quadrant (superolateral) B. upper inner (superomedial) C. lower inner (inferomedial) D. lower outer (inferolateral) A | B ----- C | D
chromosomal mis-segregration occur which stage of mitosis
metaphase
note: checkpoint kinase inhibitors are used in anti-cancer therapy => inhibit spindle assembly checkpoint @metaphase
inhibitor e.g. Taxane, cause premature mitosis, chromosomal mis-segregation and apoptosis
why RBC tend to burst aka lyse in low tonicity/ why WBC got more resistance
RBC no ATP bro. no energy unlike WBC. cannot transport Na+ out of cell which controls the water potential remember???
Na+/K channel is the osmolarity controller
hydrostatic pressure vs colloid pressure which direction
google it. but to describe:
colloid is outside vessel to inside
hydrostatic is inside vessel to outside vessel
tonicity vs osmolarity
osmolarity takes into account the total concentration of penetrating solutes and non-penetrating solutes, whereas tonicity takes into account the total concentration of non-freely penetrating solutes only.
tldr: tonicity care about semi-permeable membrane
what is SLE
Systemic lupus erythematosus. immune system attacks its own tissues, causing widespread inflammation and tissue damage in the affected organs. It can affect the joints, skin, brain, lungs, kidneys, and blood vessels.
what are the 7 oncoviruses?
hep B, hep C, human T lymphotropic virus, merkel cell polyomavirus, human papillomavirus, Epstein Barr virus, HHV-8
what are the associated cancers for the 7 oncovirus?
hep b, hep c, human t lymphotropic virus, merkel cell polyomavirus, HPV, HHV-8, Epstein-Barr
hep b -> hepatocellular carcinoma
hep c -> hepatocellular carcinoma
human t lymphotropic virus (HTLV) -> adult T cell leukaemia
merkel cell polyomavirus -> merkel cell carcinoma
ebstein barr virus -> burkitt’s lymphoma, hodgkin’s lymphoma
HHV-8 -> kaposi’s sarcoma
human papillomavirus -> cervical cancer, anal cancer, etc,
!!! hep c and HTLV RNA virus , the rest DNA
RAS pathway. what are the steps
peptide growth factors -> tyrosine kinase receptors -> receptor dimerise and cross phosphorylate -> recruit adaptor and signaling protein Grb2 + Sos (protein/exchange factor) -> RAS GTP binding protein activated -> exchange of GDP for GTP -> active (bound to plasma membrane) Ras protein -> activate protein kinase cascade
protein kinase cascade:
activated kinase 1 [RAF, MAPKKK] use gamma phosphate in ATP phosphorylate kinase 2 [MEK, MAPKK] -> kinase 2 use ATP phosphorylate kinase 3 [ERK, MAPK]
MAPK: mitogen-activated protein kinase
Herceptin is what
anti-HER2 antibody. block the HER2 receptor tyrosine kinase
cyclin dependent kinases (CDK) at M, G and S phase
M phase: cdk1 + cyclin B = m-cdk (MPF= m-phase promoting factor)
G phase: cdk2 + cyclin E = G1/S-cdk
S phase: cdk2 + cyclin A = S-cdk
whats the point of ERK
ERK phosphorylates and upregulate expression of Myc to express cyclin D. cyclin D bind to cdk4/6 and Rb protein to release E2F transcription factor
cyclin E transcribed -> bind to cdk2 -> drive G1 to S phase
cdk2-cyclinE phosphorylate Rb -> release more E2F -> transcribe cyclin A
cyclin A -> bind to cdk2 -> enter S phase
rice water stools means kena what
cholera
^ will have increased cAMP cause Cl- EFflux into gut lumen
note: usually presented with no blood in faeces.
cholera presents with large volume losses -> fluid loss, electrolyte loss
watery diarrhoea means what
what can cause it
non invasive, increased secretion of water and electrolytes
causes:
bacteria - vibrio cholerae, ETEC (E. coli), S. aureus
virus - norovirus, rotavirus
parasite- giardia duodenalis aka giardia intestinalis/lamblia (the parasite look like face LOL)
bloody diarrhoea means what
caused by what
invasive; pathogenesis includes toxins that kill enterocytes
causes:
bacteria- shigella dysenteriae, EHEC (E. coli), Salmonella spp, Campylobacter jejuni (curved, look like w)
parasites- entamoeba histolytica
complication of cholera
hypokalemic metabolic acidosis
CD8+ T cell recognize what type of antigen (exogenous or endogenous) on what MHC
endogenous on MHC1
cd8 are your cytotoxic!!! they release the granzymes and perforin so then the cell so poof. they kill those 不是自己人
T cells cells diff: T cells recognise exogenous on MHC2!!
to inhibit Treg to reduce immunosuppression
anti CTLA-4 antibody: ipilimumab, tremelimumab
^ downregulation of out competition of CD28 binding to B7 (inhibits T cells)
anti PD-1 antibody: nivolumab, pembrolizumab
anti PD-L1 antibody: MPDL3280A
^ downregulation of PD-1 (Effector T cell) and PD-L1 (Treg/tumour cell) binding
therefore, more T cell, higher immuno :D
Beri-beri caused by what
deficiency of vitamin B1
problem with TPP (pyruvate dehydrogenase complex)
beta oxidation what 4 steps.
what do u get in the first step of b-oxidation
OHOT
oxidation, hydration, oxidation and thyolisis (aka cleavage)
first step: acyl CoA
last step: 2 acetyl CoA
what are some tumour suppressor genes?
p53, bRCA1, PTEN, APC, p16 INK4a, MLH1
function, location and associated cancer of the tumour suppressor genes
p53, BRCA1, PTEN, APC, p16 ink4A, MLH1
p53 -> cell cycle regulator, nuclear, many e.g. colon, breast, bladder, lung
BRCA1 -> cell cycle regulator, nuclear, breast & ovarian & prostate
PTEN -> tyrosine and lipid phosphatase, cytoplasmic, prostate & glioblastoma
APC -> cell signaling, cytoplasmic, colon
p16ink4A-> cell cycle regulator, nuclear, colon and others
MLH1 -> mismatch repair, nuclear, colon and gastric
initiator caspases that trigger cell death programme (apoptosis)
effector caspases that carry out later stages of cell death (apoptosis)
initiator: caspase 2, caspase 9, caspase 10, caspase 8
effector: caspase 3, 6, 7
four hypersensitivity types
Type I: reaction mediated by IgE antibodies.
* allergic rhinitis. degranulation of mast cells, release of histamine, asthma
Type II: cytotoxic reaction mediated by IgG or IgM antibodies.
*Graves disease, overactivated thyroid! not thymus! THYROID. autoimmune disease
Type III: reaction mediated by immune complexes.
*Rheumatoid arthritis, SLE
Type IV: delayed reaction mediated by cellular response.
*poison ivy rash, Rheumatoid arthritis
allergic asthma is what type of INFLAMMATION
**not hypersensitivity
type 1/4
graves disease, rheumatoid arthritis, poison ivy what type of hypersensitivity
graves disease-> type 2
rheumatoid arthritis-> type 3
poison ivy rash -> type 4
DiGeorge syndrome is what
highest concentration of IgM, have hypoplastic/absent thymus. T cell cannot mature, therefore no class switching to B cell. therefore, only IgM produced
what type of necrosis associated with acute pancreatitis
fat necrosis.
pancreatic lipase leak out of pancreas to digest fat in the abdomen. fatty acids produced can combine with calcium to form visible chalky deposits
what are 1. coagulative necrosis 2. caseating necrosis 3. fibrinoid necrosis 4, liquefactive necrosis 5. fat necrosis associated with
- infarction in solid organs, other than the brain e.g. myocardial infarction
* proteins denature -> form gelatinous substance -> maintain tissue architechture - tuberculosis, looks like cheese
* dead cells disintegrate but no completely digested -> soft, white proteinaceous mass of granular debris walled off by a distinctive inflammatory border (grannuloma) - deposition of antigen-antigen complexes within blood vessel
- hypoxic infarcts in BRAIN
* dead cells digested by own enzymes -> viscous, liquid mass in cystic space (abscess formation) - acute pancreatitis
* activated lipase necrose fat tissue -> lesion can bind calcium to product soap/ calcium deposits
atrial fibrillation complication
cerebrovascular attack.
AF due to to arrhythmias cause stasis, create thrombus in left atrium. then reach brain where occludes (stroke)
characteristics of DVT:
____in extremities. ____ lodge within pulmonary artery -> cause _____ -> cause ____-> cause _____ since heart try to pump harder
varicosities in extremities. thrombus lodge within pulmonary artery -> cause pulmonary embolism -> cause pulmonary hypertension -> cause right ventricular failure since heart try to pump harder
lobar pneumonia caused by what
usually bacterial infection.
less common: viral/fungal
treatment: antimicrobial therapy
which pneumonia associated with
- haemophilus influenza
- staph aureus
- strep cocci/pneumococci
- TB
- pneumocytis jiroveci
- aspergillus
- influenza, adenovirus, varicella
- bronchopneumonia
* virus, has fimbriae, hair-like structure to anchor on airway epithelial cells to prevent removal by mucociliary clearance - bronchopneumonia
- bronchopneumonia and lobar pneumonia
- bronchopneumonia
- interstitial pneumonia
* fungi, usually in severely immune suppressed individuals - interstitial pneumonia
- interstitial pneumonia
bronchiectasis is what, symptoms got what
bronchiectasis vs bronchitis
bronchiectasis: chronic, necrotising infective inflammatory condition => permanent irreversible dilatation of airways
bronchitis: inflammation of mucous membrane in bronchi
symptoms:
bronchiectasis - green/brown/blood-stained sputum (blood due to necrosis and infection), chocolate brown material in bronchiole wall since decreased elastin
bronchitis - white to yellow mucous, only if super infected then green to brown mucous, less sputum than bronchiectasis
root of right lung (hilum) posterior anterior got what
posterior: azygous vein
anterior: SVC
thoracic aortic aneurysm can lead to compression of what
thoracic duct and oesophagus
note: thoracic duct ascend through aortic hiatus, right of the aorta and cross to the left (posterior to oesophagus at T5)
use of accessory muscles for inspiration implies what
inability to use diaphragm (cannot contract) and thus, phrenic nerve injury => raised hemidiaphragm
phrenic nerve supply what
fibrous pericardium, diaphragmatic peritoneum, parietal pleura,
kussmaul respiration is what
deep, regular sighing breaths with any rate, represent respiratory compensation for metabolic acidosis (low bicarbonate)
women go mountain, lung how change
high altitude -> low o2 level -> HPV -> increased pulmonary resistance
due to low pAo2 -> alveolar ventilation -> reduction of PaCO2, increase pH, o2 curve shift left (respiratory alkalosis)
compensation:
respiratory alkalosis - renal compensation -> alveolar ventilation -> pao2 rise -> pH return
o2 curve shift left - RBC glycolysis -> increased production of 2,3-DPG, binds allosteric site of globin chain -> stabilize low affinity state -> shift o2 curve to RIGHT (facilitate tissue unloading)
increased hematocrit (no. of RBC) since lesser o2, stroke volume = CO x TPR and heart rate increase
pink frothy sputum means what
pulmonary oedema: will have impaired gas exchange, reduced lung compliance, increased pulmonary venous pressure
other symptoms: terrified, severe SOB, crackles heard upon auscultation (since inspiration opens alveoli with fluid)
o2 curve shift left vs right
left: loading of o2 (higher affinity of hb)
right: unloading of o2 (lower affinity of hb)
causes for o2 curve shift left
+ where
left:
increased pH (alkalosis)
reduced PaCO2 (bohr effect)
reduced body temp
foetal Hb, pulmonary capillaries
note: shift right just switch opposite
- maternal hb, and stored blood (detrimental), metabolically active tissue (unload o2)
sleep vs awake
when awake, tidal volume increases!! more respiratory muscles used when breathing (more effort)
other effects! but less
alveolar ventilation increases (increased respiratory effort)
SaO2 of arterial blood increases slightly
PaCo2 of venous blood decreased (body doesnt reach apnoeic threshold before stimulation of breathing)
breathing rate increases
stroke volume or Pao2 reduction by 20% more jialat
stoke volume reduction
!! only 2% of o2 transported in blood is in PaO2, 98% bound to Hb.
!!! 20% drop of SV means 20% drop of o2 delivery
contraction of diaphragm during inspiration or expiration
EXPIRATION BODOH
how to expire at super fast speed zoom zoom
breath in larger initial volume before breathing out
how much blood loss and what class
HR <100, BP and PP normal, RR 14-20
UOP >30, CNS slightly anxious
class 1, <740ml ~15% blood loss
how much blood loss and what class
HR >100, BP normal, PP decrease, RR 20-30
UOP 20-30, CNS madly anxious
class 2, 750ml-1500ml 15%-30% blood loss
note: normal blood ~5000ml
how much blood loss and what class
HR >120, BP and PP decrease, RR 30-40
UOP 5-15, CNS anxious confused
class 3, 1500-2000ml 30-40% blood loss
how much blood loss and what class
HR >140, BP and PP decrease, RR >35
UOP negligible, CNS confused and lethargic
class 4 >2000ml >40% blood loss
RAA system describe
angiotensinogen -> angiotensin 1 (enzyme: renine)
angiotensin 1 -> angiotensin 2 (enzyme: ACE)
bradykinin decrease -> NO decrease -> vasoconstriction
AT2 bind to AT1 -receptor -> release aldosterone -> retain SODIUM
OVERALL EFFECT: INCREASED BLOOD PRESSURE
types of shock (4 types)
hypovolaemic, cardiogenic, distributive, obstructive
note: distributive * septic shock, anaphylactic shock cardiogenic * dysfunction of heart muscle, inability to pump and supply blood to organs
anterior infarct which lead have ST elevation
V1, V2, V3 and V4
which lead ST elevation for lateral infarct
lead I, V5, V6, aVL
Von Willebrand disease is what
primary haemostatic disease.
epistaxis, prolonged gum bleed, menorrhagia (menstruation longer than 7 days), easy bruising
Von Gierke’s disease is what
2 mutant copies of G6Pase (glucose-6-phosphatase) gene inherited. one from each parent -> G6Pase deficiency
characteristics -> low blood sugar, slow growth, large livers, short stature
Von Gierke’s disease is what
2 mutant copies of G6Pase gene inherited. one from each parent -> G6Pase deficiency
characteristics -> low blood sugar, slow growth, large livers, short stature
Barrett’s esophagus is what
metaplasia!!
non-keratinised stratified epithelial cells replaced by simple columnar epithelial cells when exposed to stomach acid (E.G. during stomach acid reflux)
note: metaplasia is reversible!!
anomaly during metaphase -> daughter cells have unequal amount of DNA
deficiencies in BUB kinase signaling
- BUB kinase generate checkpoint signals during metaphase when kinetochores are not bound to microtubules
- prevent anaphase from taking place until all kinetochore attached to MT
- deficiency = premature anaphase
amphitelic attachment of microtubule to chromosome kinetochore normal anot
yes. amphitelic literally means proper attachment of spindle attachment
abberrant cytokinesis -> unequal amount of DNA occurs when
cytokinesis AFTER mitosis
transcription of DNA occur which direction
5’ to 3’
binding of elF2 to GTP and Met-tRNA involved in what process
translation!!
what is profilin
profilin = protein assist microfilament elongation
*exchanges ADP for ATP on actin monomers -> convert to readily polymerizing form
how does polymerisation of MT occur
nucleation: require tubulin, Mg, GTP, 37 degrees. SLOW
elongation: polymerisation of dimer, happens at PLUS END if GTP present
note: MT does not keep growing if GDP is at the plus end
5 types of intermediate filament
type 1 and 2: acidic keratin (type 1) and basic keratin (type 2)
* found in epithelial cells (bladder, skin, etc)
type 3: cell types include
- vimentin (fibroblasts, endothelial cells, leukocytes)
- desmins (desmosomes e.g. cardiac muscle, skeletal muscle)
- glial fibrillary acidic protein GFAP (in astrocytes)
- peripherin (peripheral nerve fibers)
type 4: neurofilament
- heavy, medium, low
- modifiers refer to molecular weight of protein, mainly in axonal cells
type 5: lamins
- filamentous support inside inner nuclear membrane
- vital for reformation of nuclear envelope after cell division
what does gelsolin do to microfilament aka actin
gelsolin binds to +end!
gelsolin involved in severing and capping microfilament -> increase number of filaments avail -> increase TOTAL RATE of elongation
note:
ARP 2/3 and WASP assist in nucleation of microfilament
filamin assist microfilament bundling
prokaryote DNA replication how many origin
ONLY ONE. remember its a CIRCLE!! so only form ONE replication bubble